What are the causes of pulmonary edema?

Causes of Pulmonary Edema

Pulmonary edema develops through two fundamental mechanisms: elevated hydrostatic pressure (cardiogenic) or increased capillary permeability (non-cardiogenic), with the critical distinction determining treatment approach. 1

Cardiogenic Causes (Elevated Hydrostatic Pressure)

The primary mechanism involves elevated left ventricular filling pressure transmitting backward into pulmonary capillaries, forcing fluid into the interstitium and alveoli when pulmonary capillary wedge pressure exceeds plasma oncotic pressure (typically >18 mmHg). 1, 2

Acute Cardiac Events

• Acute myocardial infarction or injury creates sudden ventricular dysfunction with elevated left ventricular filling pressure and increased pulmonary capillary wedge pressure. 1
• Decompensated heart failure from any cause results in inadequate cardiac output with compensatory fluid retention and elevated filling pressures. 1
• Cardiac arrhythmias (particularly supraventricular tachycardia) impair ventricular filling or reduce cardiac output, leading to pulmonary congestion. 1

Structural Heart Disease

• Valvular disease, particularly aortic stenosis and mitral regurgitation, creates pressure or volume overload that transmits backward into pulmonary veins. 1
• Cardiomyopathy of any etiology increases capillary hydrostatic pressure through impaired ventricular function. 1
• Pericardial disease restricts cardiac filling and elevates venous pressures. 1

Volume Overload States

• Renal failure increases capillary hydrostatic pressure through volume overload. 1
• Cirrhosis with portal hypertension elevates hydrostatic pressure. 1
• Excessive fluid administration represents an iatrogenic cause that aggravates existing lung injury. 1

Non-Cardiogenic Causes (Increased Capillary Permeability)

Inflammatory mediators cause endothelial cell contraction and disruption, creating gaps in the capillary membrane that allow protein-rich fluid to leak into the interstitium and alveoli, with PCWP remaining <18 mmHg. 1, 3

Inflammatory/Infectious Causes

• Sepsis and ARDS represent prototypical non-cardiogenic causes where inflammatory mediators increase capillary permeability. 1
• Upper respiratory infections progress to pulmonary edema through sepsis or ARDS, with 28-33% of septic patients meeting ARDS criteria when clinical manifestations first appear. 3
• The inflammatory process eliminates the protective oncotic gradient by allowing oncotic molecules to cross freely, promoting extravascular lung water accumulation. 1

Environmental Causes

• High-altitude exposure causes pulmonary edema in 40-60% of mountaineers through mechanisms including subclinical edema and increased cough-receptor sensitivity. 1
• Pulmonary embolism causes cough and edema in nearly half of documented cases. 1

Iatrogenic Causes

• Blood product transfusions and injurious mechanical ventilation aggravate existing lung injury as "second hits." 1

Post-Procedural Causes

• Re-expansion pulmonary edema occurs after rapid removal of air or pleural fluid from the pleural space, believed to result from increased capillary permeability related to mechanical forces causing vascular stretching during re-expansion or ischemia-reperfusion injury. 4

Special Circumstances

Diabetic Ketoacidosis

• Hypoxemia and noncardiogenic pulmonary edema may complicate DKA treatment, attributed to reduced colloid osmotic pressure that increases lung water content and decreases lung compliance. 4
• Patients with widened alveolo-arteriolar oxygen gradient on initial blood gas or pulmonary rales on examination are at higher risk. 4

Low Alveolar Pressure

• Upper airway obstruction (laryngeal paralysis, strangulation) creates negative alveolar pressure that draws fluid into alveoli. 5

Neurogenic Edema

• Epilepsy, brain trauma, and electrocution can trigger neurogenic pulmonary edema through sympathetic surge mechanisms. 5

Critical Diagnostic Distinction

The fundamental clinical task requires distinguishing elevated cardiac filling pressures from normal pressures with increased permeability, as treatment differs markedly between the two. 1, 5

• Pulmonary artery catheterization definitively measures PCWP: >18 mmHg suggests cardiogenic, <18 mmHg suggests non-cardiogenic. 1
• Echocardiography objectively assesses ventricular function, wall motion abnormalities, and valvular disease. 1
• B-natriuretic peptide or NT-proBNP elevation suggests cardiac etiology, though obesity and renal failure affect levels. 1